[Lotus]

Thanks lotus you have given me a few things to think about, im due my next decapeptyl shot next week, i will probably wait a week or two then see if i can get some blood tests done, probably estradiol, testosterone, prolactin, LH and FSH, i have to be a bit careful what i ask for, i wont do anything differently until after i have my blood results, btw i thought progesterone was meant to also raise prolactin or is that only in high dose? i have a some 100mg utrogestan capsules that i had planned to start at some point

They (prolactin and progesterone) off-set each other, but I've seen a studies (or 2) when they've been introduced at the same time they synergistically upregulated estrogen, so go figure lol, good luck on trying to achieve that balance. ok Bobie, good luck, please let me know how it goes.

Vitex inhibits prolactin levels by binding to dopamine D2 receptors in the pituitary

Prolactin and dopamine: what is the connection? A review article.
Fitzgerald P1, Dinan TG.
Author information
Abstract
Dopamine (DA) holds a predominant role in the regulation of prolactin (PRL) secretion. Through a direct effect on anterior pituitary lactotrophs, DA inhibits the basally high-secretory tone of the cell. It accomplishes this by binding to D2 receptors expressed on the cell membrane of the lactotroph, activation of which results in a reduction of PRL exocytosis and gene expression by a variety of intracellular signalling mechanisms. The hypothalamic dopaminergic neurons, which provide DA to the anterior pituitary gland, are themselves regulated by feedback from PRL through a 'short-loop feedback mechanism'. A variety of other modulators of prolactin secretion act at the hypothalamic level by either disinhibition of the dopaminergic tone (e.g. serotonin, GABA, oestrogens and opioids) or by reinforcing it (e.g. substance P). All typical antipsychotic medications are associated with sustained hyperprolactinaemia due to their high affinity for the D2 receptor and their slow dissociation from the receptor once bound, but atypicals differ quite dramatically in their propensity to cause prolonged high prolactin levels. Of those atypicals that are associated with prolactin elevation, the main causative factor appears to be a higher peripheral-to-central dopamine receptor potency of either the parent drug or its active metabolite (e.g. risperidone, 9-hydroxy-risperidone and amisulpride). Antipsychotics that easily cross the blood-brain barrier and exhibit fast dissociation from the dopamine receptor once bound do not result in sustained hyperprolactinaemia.